From the Department of Neurology, Georg-August-University, Göttingen
(A.B., W.K., L.M., H.P.), and Department of Neurology,
Julius-Maximilians-University, Würzburg (P.R.) (Germany).
Correspondence to Dr Andreas Bitsch, Klinik und Poliklinik für Neurologie, Robert-Koch-Straße 40, 37075 Göttingen, Germany. E-mail abitsch{at}t-online.de
Background and
Purpose—Activation of endothelial cells is a
consequence of cerebral ischemia and leads to the expression of
adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1),
vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, which can
be released into the blood. This study aimed to define the kinetics of
soluble adhesion molecule serum levels after cerebral ischemia
and their correlation with the extent of neurological deficits,
clinical outcome, and infarct volume as measured on CT scans.
Methods—Plasma levels of soluble (s) ICAM-1, sVCAM-1, and
sE-selectin were repeatedly determined by ELISA in 38 patients during a
period of 14 days after acute cerebral ischemia.
Results—Soluble adhesion molecule levels demonstrated
considerable variability. Overall, concentrations revealed
characteristic and significant changes after completed strokes but not
after transient ischemic attacks. In patients with completed
stroke (n=26) but not in patients with transient ischemic
attacks (n=12), sICAM-1 peaked within 24 hours (P=0.04),
sVCAM-1 reached a maximum after 5 days (P=0.02), and
sE-selectin levels decreased after 5 days (P=0.002).
There was no clear-cut correlation of soluble adhesion molecule levels
with infarct volume or clinical disability. The initial increase of
sE-selectin levels was higher in more disabled patients
(P=0.02). sICAM-1 levels were higher in patients with
signs of infection (n=9; P=0.03).
Conclusions—As a result of large interindividual variability
influenced by ischemia-independent factors, soluble adhesion
molecules are not reliable candidates as surrogate markers in acute
cerebral ischemia. The characteristic profile of individual
soluble adhesion molecules after completed stroke supports prior
hypotheses of their involvement in the pathogenesis of acute cerebral
ischemia, but this needs to be clarified in detail.
© 1998 American Heart Association, Inc.
Original Contributions
A Longitudinal Prospective Study of Soluble Adhesion Molecules in Acute Stroke
Key Words: cell adhesion molecules • cerebral ischemia, transient • selectins • stroke
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